Regulatory T Cells Can Mediate Their Function through the Stimulation of APCs to Produce Immunosuppressive Nitric Oxide
| Autor: | Lingwen Zhong, Cyndi Chen, Wen-Hui Lee, Chih-Pin Liu |
|---|---|
| Rok vydání: | 2006 |
| Předmět: |
Immunology
Cell Population Antigen-Presenting Cells Cell Communication Cell Separation Biology Nitric Oxide T-Lymphocytes Regulatory Diabetes Mellitus Experimental Immune tolerance Interferon-gamma Mice Interleukin 21 Immune Tolerance medicine Animals Immunology and Allergy IL-2 receptor Antigen-presenting cell education Cells Cultured education.field_of_study CD40 Th1 Cells Adoptive Transfer Phenotype Cell biology medicine.anatomical_structure biology.protein |
| Zdroj: | The Journal of Immunology. 176:3449-3460 |
| ISSN: | 1550-6606 0022-1767 |
| DOI: | 10.4049/jimmunol.176.6.3449 |
| Popis: | Regulatory T cells (Tr cells) play a critical role in inducing immune tolerance. It remains largely unclear how various types of Tr cells perform their regulatory function. We have studied the underlying regulatory mechanism of a population of autoantigen-specific CD4+ Tr cells. These T cells are specific for the glutamic acid decarboxylase p206–220 peptide and are isolated from the diabetes-resistant nonobese-resistant mice. Although these T cells express T-bet and display a Th1 phenotype, they are able to inhibit diabetes. Their regulatory function is dependent on both IFN-γ and cell contact with target cells. These Tr cells can mediate their cell contact-dependent regulatory function by secreting IFN-γ which stimulates APCs to produce NO. NO is necessary for the Tr cells to inhibit the proliferation of pathogenic T cells and the development of diabetes. Therefore, we have identified a novel mechanism by which these Tr cells can exert their regulatory function. These results also provide an explanation as to why IFN-γ may play both pathogenic and immunomodulatory roles in autoimmune diseases. |
| Databáze: | OpenAIRE |
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